May 2015 FACT SHEET

GLYPHOSATE AND CANCER RISK: FREQUENTLY ASKED QUESTIONS

WHY IS THERE CONCERN ABOUT showing higher rates of cancer in glyphosate-using GLYPHOSATE AND CANCER? The World farmers; and research showing that glyphosate damages Health Organization’s (WHO’s) cancer authorities – the DNA and chromosomes, one mechanism by which cancer International Agency for Research on Cancer (IARC) is induced.2 IARC’s full assessment is due out in 2016. – recently determined that glyphosate is “probably carcinogenic to humans” (Group 2A). Glyphosate is WHOSE ASSESSMENT IS MORE the most heavily used pesticide in the world thanks to RELIABLE: IARC OR EPA? IARC is the world’s widespread planting of Monsanto’s Roundup Ready crops, leading authority on cancer. Its glyphosate determination which are genetically engineered to survive spraying with was made by unanimous decision of 17 qualified scientists it. Use and exposure will increase still more if glyphosate- led by Dr. Aaron Blair, a distinguished epidemiologist resistant turfgrasses currently being developed for lawns, recently retired from the U.S. National Cancer Institute.3 playing fields and golf courses are introduced. IARC’s assessment is up-to-date, analyzing all the relevant available research, while EPA’s last comprehensive WHERE DO EPA AND WHO’S IARC STAND assessment of glyphosate occurred in 1993. IARC ON GLYPHOSATE’S CARCINOGENICITY? considered a broad range of evidence, including human In 1985, EPA classified glyphosate as a possible epidemiology and other peer-reviewed studies, while EPA carcinogen based on experiments showing tumors in did not assess epidemiology and relied almost entirely on glyphosate-treated rodents. Input from Monsanto led to unpublished industry studies.4 IARC is an independent a dubious reinterpretation of these studies by EPA, and agency whose sole mission is human health. While EPA reclassification of glyphosate as non-carcinogenic in is charged with protecting human health as well, it is also 1991.1 IARC has thus far published only a brief summary subject to considerable pressure from pesticide companies of its glyphosate assessment, which is based on multiple whose products it regulates. EPA is currently re-assessing lines of evidence: kidney, pancreatic and other tumors glyphosate, and has said it will consider IARC’s findings. in glyphosate-treated test animals; epidemiology studies

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HOW DOES GLYPHOSATE COMPARE TO IS THE GENERAL PUBLIC AT RISK FROM OTHER AGENTS THAT CAUSE OR MAY GLYPHOSATE? Because of glyphosate’s extremely CAUSE CANCER? The evidence implicating intensive use (300 million lbs./year, more than four times glyphosate as a human carcinogen is not as strong as that that of the second-leading pesticide, atrazine), it is regularly for smoking or asbestos (IARC Group 1, “carcinogenic”), found in food (e.g. bread), the air, rainfall and surface but stronger than that for DDT, parathion (both waters.12 Glyphosate is found at similar frequencies and insecticides) or infection with type 2 HIV virus (Group levels in the urine of farm and non-farm family members, 2B, “possibly carcinogenic”).5 including children, suggesting similar levels of exposure.13 Glyphosate has also been detected in human blood.14 E PA’s BUT DOESN’T IARC CONSIDER SUNLIGHT maximal “safe” level of glyphosate exposure is six times AND ALCOHOL TO BE CARCINOGENIC? higher than Europe’s,15 and 17.5-fold higher than the level Although IARC primarily assesses chemicals, it also EPA itself set in the early 1980s.16 EPA’s latest high-end evaluates the carcinogenic potential of other “agents,”6 estimate of infant exposure to glyphosate exceeds the level it which has unfortunately been used by some in a misguided regarded as safe in the 1980s;17 and is five times higher than attempt to cast doubt on its glyphosate determination. In the maximum level suggested by independent scientists.18 fact, IARC’s classifications of UV radiation and alcohol as “carcinogenic” are well-supported by science. Dermatologists ARE THERE OTHER PROBLEMS WITH regard excessive exposure to UV radiation (a component of GLYPHOSATE ASSESSMENTS? EPA’s sunlight) as the most important preventable cause of skin assessments of glyphosate share the weaknesses of all the cancer.7 According to the American Cancer Society, “alcohol Agency’s pesticide regulation. Most testing has involved is a known cause of cancers” of eight different organs.8 The only the active ingredient glyphosate, even though point is not that sunshine or drinking a few beers will kill formulations (e.g. Roundup) used in the real world are you, but that you can reduce your risk of cancer by avoiding often more toxic due to the presence of additional, often frequent sunburns and cutting back on heavy drinking. One undisclosed, ingredients.19 While we are all exposed to important distinction here is that you can choose to wear multiple pesticides in our food, water and air, EPA does sunscreen or drink less, but for most of us it is difficult to not consider the additive or synergistic effects of exposure reduce our exposure to chemicals like glyphosate. to glyphosate together with other pesticides. Finally, EPA’s practice of basing its decisions almost entirely on IS IARC’S ASSESSMENT RELEVANT TO studies conducted or commissioned by the pesticide ACTUAL HUMAN RISK OF CANCER? registrant introduces serious conflicts of interest,20 and A formal risk assessment evaluates both the inherent excludes pertinent evidence from peer-reviewed studies toxicity of a substance (called hazard) and our exposure by independent scientists.21 to it. While a toxic substance is always hazardous, the risk it poses depends upon the circumstances of exposure.9 DO OTHER HERBICIDES POSE CANCER While IARC does not directly evaluate exposure (it is a RISKS? Massive use of glyphosate with Roundup Ready hazard assessment), it does consider the results of qualified crops has generated an epidemic of glyphosate-resistant epidemiological studies, which evaluate risk from actual weeds. In response, pesticide companies are poised to exposure under real-world conditions. Three epidemiology introduce a host of “next-generation” GE crops resistant to studies of farmers show a link between glyphosate and herbicides such as 2,4-D and dicamba as well as glyphosate. non-Hodgkin’s lymphoma (NHL), an immune system These new GE crops will trigger an unprecedented and cancer.10 Another finds a “suggestive association” between increasingly toxic spiral of weed resistance and herbicide glyphosate and a related immune system cancer, multiple use in American agriculture, for instance, a several- myeloma (but not NHL), and recommends follow-up given fold rise in 2,4-D and dicamba applications, with no the herbicide’s widespread use.11 Because there is typically a countervailing reduction in glyphosate.22 Exposure to time lag of decades between exposure to a carcinogen and 2,4-D and dicamba is linked to non-Hodgkin’s lymphoma elevated cancer rates, and glyphosate use has skyrocketed (NHL), the same cancer with which glyphosate has been over the past 10-15 years, the full effects of glyphosate’s associated.23 Herbicide exposure in general is also linked rising use remain to be discovered. to increased rates of Parkinson’s disease.24 PESTICIDES & GE CROPS

ENDNOTES S

1 EPA (1991). Memorandum on Second Peer Review of Glyphosate, U.S. Environmental 13 Curwin BD et al. (2007a). Urinary pesticide concentrations among children, mothers Protection Agency, 10/30/91. and fathers living in farm and non-farm households in Iowa. Ann. Occup. Hyg. 51(1): 53- 2 Guyton KZ et al. (2015). Carcinogenicity of tetrachlorvinphos, parathion, malathion, dia- 65; and Curwin BD et al. (2007b). Pesticide dose estimates for children of Iowa farmers and zinon, and glyphosate. Lancet Oncology (March 20th), doi:10.1016/S1470-2045(15)70134- non-farmers. Environmental Research 105: 307-315. For Europe, see FoEE (2013). Human 8. contamination by glyphosate. Friends of the Earth Europe, June 2013. 3 Pollack A (2015). Weed killer, long cleared, is doubted. New York Times 3/27/15; and 14 Aris A, Leblanc S. Maternal and fetal exposure to pesticides associated to genetically Gillam C (2015). Scientist defends WHO group report linking herbicide to cancer. Reuters modified foods in Eastern Townships of Quebec, Canada. Reprod Toxicol. 2011: 31(4): 3/26/15. 528-533. 4 EPA (1993). Glyphosate Reregistration Eligibility Decision. U.S. Environmental Protec- 15 “Acceptable daily intake” (ADI) or the equivalent “chronic population adjusted dose” tion Agency, Sept. 1993, App. C. (cPAD), expressed as milligrams glyphosate per kilogram body weight per day: 0.3 in Eu- 5 See IARC List of classifications at http://monographs.iarc.fr/ENG/Classification/index. rope vs. 1.75 mg/kg/day in the U.S. For Europe, see http://ec.europa.eu/food/plant/protec- php. tion/evaluation/existactive/list1_glyphosate_en.pdf, Appendix II; for US, see EPA (2006). 6 IARC also assesses biological organisms (e.g. viral infections), behavioral practices (e.g. Glyphosate human health risk assessment for proposed use on Indian mulberry and amend tobacco smoking), occupational exposure (e.g. as firefighter), physical agents (e.g. surgical use on pea. EPA, 9/29/06, p. 21. implants), and foods or components of food (e.g. coffee and caffeine), collectively referred 16 For EPA’s setting of the glyphosate ADI at 0.1 mg/kg/day in the early 1980s (vs. 1.75 to- to as “agents.” See IARC Monongraphs on the Evaluation of Carcinogenic Risks to Humans, day), see EPA (1983). Glyphosate (Roundup) on wheat. March 3, 1983. Preamble, at http://monographs.iarc.fr/ENG/Preamble/CurrentPreamble.pdf. 17 See EPA (2006) in footnote 14, Table 6.1.2, maximum infant exposure = 0.127562 mg/ 7 American Academy of Dermatology: Melanoma FAQs. https://www.aad.org/media-re- kg/day, 28% higher than the 1980’s ADI of 0.1 mg/kg/day (see EPA 1983 in last footnote). sources/stats-and-facts/conditions/melanoma-faqs. 18 Antoniou M et al. (2012). Teratogenic effects of glyphosate-based herbicides: diver- 8 American Cancer Society: Alcohol Use and Cancer. The organs are the mouth, throat, gence of regulatory decisions from scientific evidence. J Environ Anal Toxicol S4:006. larynx, esophagus, liver, colon, rectum and breast, see: http://www.cancer.org/cancer/can- doi:10.4172/2161-0525.S4-006, suggesting an ADI of 0.025 mg/kg/day based on teratogenic cercauses/dietandphysicalactivity/alcohol-use-and-cancer. rather than carcinogenic effects. 9 Key factors include the timing and level of exposure. Children and fetuses are generally 19 See references at: http://earthopensource.org/gmomythsandtruths/sample-page/4- more susceptible to harm than adults; and while greater exposure is generally thought to health-hazards-roundup-glyphosate/4-2-myth-strict-regulations-ensure-exposed-safe- mean greater risk, lower levels of hormone-disrupting chemicals sometimes cause more levels-roundup/ harm than higher levels (Vandenberg LN et al. 2012. Hormones and endocrine-disrupting 20 Boone MD et al. (2014). Pesticide regulation amid the influence of industry. BioScience chemicals: low-dose effects and nonmonotonic dose responses. Endocrine Reviews 33(3): 64: 917-922. 378-455). 21 Myers JP et al. (2009). Why public health agencies cannot depend on good laboratory 10 Guyton et al., 2015. practices as a criterion for selecting data: the case of bisphenol A. Environmental Health 11 De Roos AJ et al. (2005). Cancer incidence among glyphosate-exposed pesticide appli- Perspectives 117(3): 309-315. cators in the Agricultural Health Study. Environmental Health Perspectives 113(1): 49-54. 22 Mortensen DA et al. (2012). Navigating a critical juncture for sustainable weed manage- 12 For 2012 agricultural use of glyphosate (>280 million lbs.) and atrazine (70 million lbs.) ment. Bioscience 62(1): 75-85. in the U.S., see charts below maps at pertinent links on http://water.usgs.gov/nawqa/pnsp/ 23 Schinasi L, Leon ME (2014). Non-Hodgkin lymphoma and occupational exposure to usage/maps/compound_listing.php?year=2012&hilo=L. For non-farm uses of glyphosate agricultural pesticide chemical groups and active ingredients: a systematic review and me- (18-23 million lbs./year), see: EPA (2011). Pesticide Industry Sales and Usage: 2006 and ta-analysis. Int. J Environ. Res. Public Health 11: 4449-4527. McDuffie HH et al (2001). 2007 Market Estimates, EPA, Feb. 2011, Tables 3.7 & 3.8. For glyphosate in food, see FoEE Non-Hodgkin’s lymphoma and specific pesticide exposures in men: cross-Canada study (2013). Human contamination by glyphosate. Friends of the Earth Europe, June 2013. of pesticides and health. Cancer Epidemiology, Biomarkers & Prevention 10: 1155-1163. For lack of testing in U.S., see: Gillam C (2015). Regulators may recommend testing food 24 For instance, see: Brighina L et al. (2008). Alpha-synuclein, pesticides and Parkison dis- for glyphosate residues, Reuters, 4/20/15. For glyphosate in air, rain and surface water, see ease. Neurology 70: 1461-1469. Chang F-C et al. (2011). Occurrence and fate of the herbicide glyphosate and its degradate aminomethylphosphonic acid in the atmosphere. Environ Toxicol Chem 30(3): 548-555; and Coupe RH et al. (2011). Fate and transport of glyphosate and aminomethylphosphonic acid in surface waters of agricultural basins. Pest Manag Sci 68(1): 16-30.